scholarly journals CONTRIBUTION OF CALCIUM CURRENT TO THE VENTRICULAR ACTION POTENTIAL OF DOG

1969 ◽  
Vol 19 (6) ◽  
pp. 814-823 ◽  
Author(s):  
Ichiro MATSUBARA ◽  
Kojiro MATSUDA
Keyword(s):  
Action Potential ◽  
Calcium Current ◽  
Ventricular Action Potential

scholarly journals Contribution of L-type Ca2+current to electrical activity in sinoatrial nodal myocytes of rabbits

1999 ◽  
Vol 276 (3) ◽  
pp. H1064-H1077 ◽  
Author(s):  
E. Etienne Verheijck ◽  
Antoni C. G. van Ginneken ◽  
Ronald Wilders ◽  
Lennart N. Bouman
Keyword(s):  
Action Potential ◽  
Calcium Current ◽  
Sodium Current ◽  
Delayed Rectifier ◽  
Current Clamp ◽  
Patch Clamp Technique ◽  
Inward Current ◽  
Delayed Rectifier Current ◽  
Diastolic Depolarization ◽  
Recovery From Inactivation

The role of L-type calcium current ( I Ca,L) in impulse generation was studied in single sinoatrial nodal myocytes of the rabbit, with the use of the amphotericin-perforated patch-clamp technique. Nifedipine, at a concentration of 5 μM, was used to block I Ca,L. At this concentration, nifedipine selectively blocked I Ca,L for 81% without affecting the T-type calcium current ( I Ca,T), the fast sodium current, the delayed rectifier current ( I K), and the hyperpolarization-activated inward current. Furthermore, we did not observe the sustained inward current. The selective action of nifedipine on I Ca,L enabled us to determine the activation threshold of I Ca,L, which was around −60 mV. As nifedipine (5 μM) abolished spontaneous activity, we used a combined voltage- and current-clamp protocol to study the effects of I Ca,L blockade on repolarization and diastolic depolarization. This protocol mimics the action potential such that the repolarization and subsequent diastolic depolarization are studied in current-clamp conditions. Nifedipine significantly decreased action potential duration at 50% repolarization and reduced diastolic depolarization rate over the entire diastole. Evidence was found that recovery from inactivation of I Ca,L occurs during repolarization, which makes I Ca,L available already early in diastole. We conclude that I Ca,L contributes significantly to the net inward current during diastole and can modulate the entire diastolic depolarization.

scholarly journals Inhibition of HERG K + Current and Prolongation of the Guinea‐Pig Ventricular Action Potential by 4‐Aminopyridine

2003 ◽  
Vol 549 (3) ◽  
pp. 667-672 ◽  
Author(s):  
J. M. Ridley ◽  
J. T. Milnes ◽  
Y. H. Zhang ◽  
H. J. Witchel ◽  
J. C. Hancox
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
K Current ◽  
Ventricular Action Potential

Cytosolic magnesium modulates calcium channel activity in mammalian ventricular cells

1989 ◽  
Vol 256 (2) ◽  
pp. C452-C455 ◽  
Author(s):  
Z. S. Agus ◽  
E. Kelepouris ◽  
I. Dukes ◽  
M. Morad
Keyword(s):  
Action Potential ◽  
Calcium Channel ◽  
Action Potential Duration ◽  
Calcium Current ◽  
Concentration Addition ◽  
High Threshold ◽  
Channel Activity ◽  
Mean Values ◽  
Ventricular Cells ◽  
In Cells

The effect of cytosolic free Mg2+ concentration on the regulation of myocardial function was studied by dialyzing isolated guinea pig ventricular myocytes with different internal Mg2+ concentrations [( Mg2+]i). We found that elevation of [Mg2+]i shortened the action potential and suppressed the Ca2+ current. Mean values recorded for action potential duration in cells dialyzed with solutions containing 0, 1.3, and 9.4 mM Mg2+ were 620 +/- 40, 400 +/- 25, and 60 +/- 10, respectively. The suppressive effect of [Mg2+]i on the action potential duration correlated significantly with the suppressive effects of [Mg2+]i on the Ca2+ current. In cells dialyzed with nominally zero Mg2+, calcium current was prominent (3.5 +/- 0.58 nA). At [Mg2+]i of 1.4 mM, calcium current was significantly smaller than in zero [Mg2+]i and was almost completely inhibited by dialysis of the cell with 9.4 mM Mg2+. The Mg2+-induced block of the Ca2+ current was due to steady-state inactivation of the high threshold calcium channel. The block was observed in the presence or absence of adenosine 3',5'-cylic monophosphate and was not reversed by elevation of external Ca2+ concentration, addition of adrenaline, or large negative potentials. These data suggest that cytosolic Mg2+ regulates Ca2+ channel activity by a novel mechanism, unrelated to its effect as a blocking particle of the open channel.

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